| Project/Area Number |
18K09221
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Koga Kaori 東京大学, 医学部附属病院, 准教授 (10396723)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 子宮内膜症 / 卵巣機能 / 不妊症 |
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| Outline of Final Research Achievements |
In a study using a mouse model of endometriosis, we found that induction of endometriosis reduces the number of atomic follicles in the ovary. Using a mouse model of endometriosis, we showed that induction of endometriosis reduces the number of atomic follicles in the ovary, even in the absence of ovarian lesions or intra-abdominal lesions, and that this phenomenon is associated with the PI3K-AKT-FOXO3 pathway, as demonstrated by immunohistological staining. Furthermore, by suppressing this pathway, they were able to cancel the decrease in the number of atomic follicles.
In a study using human specimens, the PI3K-AKT-FOXO3 pathway was shown to be activated in the ovaries of endometriosis patients using immunohistological staining methods.
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| Academic Significance and Societal Importance of the Research Achievements |
子宮内膜症で卵巣機能が低下する機序として、原始卵胞の異常活性化による可能性が明らかとなった。また、原始卵胞の異常活性化の１つにPI3K/AKT経路が関与しており、PI3K/AKT阻害薬によるその卵巣機能低下が阻止される可能性が示唆された。つまり、PI3K/AKT阻害薬が子宮内膜症における卵巣機能低下への新たな治療戦略となりうると考えられた。
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